Monocyte Phenotype and Function in Patients with the Acquired Immunodeficiency Syndrome (AIDS) and AIDS‐Related Disorders

Haas, Juergen; Riethmüller, Gert; Ziegler‐Heitbrock, H. W. L.

doi:10.1111/j.1365-3083.1987.tb02269.x

Cited by 42 publications

(18 citation statements)

References 32 publications

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“…Previous studies have not identified distinct abnormalities in monocyte cell surface antigens in HIV-infected individuals (53). However, these earlier studies used a less extensive battery of mAb reagents and did not attempt to relate changes in monocyte antibacterial activity to changes in cell surface phenotype.…”

Section: Discussionmentioning

confidence: 97%

Phenotypic and functional changes in peripheral blood monocytes during progression of human immunodeficiency virus infection. Effects of soluble immune complexes, cytokines, subcellular particulates from apoptotic cells, and HIV-1-encoded proteins on monocytes phagocytic function, oxidative burst, transendothelial migration, and cell surface phenotype.

Trial

Birdsall²,

Hallum³

et al. 1995

J. Clin. Invest.

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We postulated that changes in the cell surface display of molecules that facilitate cell-cell and cell-matrix adhesions may reflect the changing immunosurveillance capacity of blood monocytes during progression of human immunodeficiency virus (HIV) infections. In Centers for Disease Control (CDC) stage A patients, whose monocytes' ability to phagocytose bacteria and generate reactive oxygen intermediates is often increased, the frequency of monocytes expressing CD49d, HLA-DP, HLA-DQ, and an activation epitope of CD11a/CD18 was increased and monocyte transendothelial migration was unimpaired. In CDC stage B/C patients, whose monocytes' ability to phagocytose bacteria and migrate across confluent endothelial monolayers was diminished, surface expression of CD49e and CD62L and the percentage of monocytes expressing CD18, CD11a, CD29, CD49e, CD54, CD58, CD31, and HLA-I were significantly decreased. Incubating normal donor monocytes with immune complexes in vitro reproduced the phenotypic and functional abnormalities seen in stage B/C patients. By contrast, in vitro stimulation with subcellular particulates released by apoptotic lymphocytes reproduced changes seen in stage A patients' monocytes. Although circulating monocytes appear to be activated at all stages, these data suggest that the high levels of circulating immune complexes, found predominantly in the later stages of HIV infection, may be particularly instrumental in reducing the monocyte's capacity to maintain surveillance against infection. (J. Clin. Invest. 1995. 95:1690-1701

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Section: Discussionmentioning

confidence: 97%

Phenotypic and functional changes in peripheral blood monocytes during progression of human immunodeficiency virus infection. Effects of soluble immune complexes, cytokines, subcellular particulates from apoptotic cells, and HIV-1-encoded proteins on monocytes phagocytic function, oxidative burst, transendothelial migration, and cell surface phenotype.

Trial

Birdsall²,

Hallum³

et al. 1995

J. Clin. Invest.

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“…Some of the differences of monocyte phenotype between HIV" and HIV* subjects, we observed, are novel (e,g, decreased proportional CD14and CDI lb expression), others were controversial (eg, up-regulation of CDlla and HLA-DR) [7][8][9][10], whereas our data on increased proportional FC7RIII expression confirm earlier reports [21], It was also previously shown that the FC7RI density was increased on monocytes from HIV* subjects [11]. We show here in addition that the proportion of Fc7RI*'"*'^'* monocytes is actually decreased in patients.…”

Section: Discussionmentioning

confidence: 99%

Expression patterns of Fcγ receptors, HLA-DR and selected adhesion molecules on monocytes from normal and HIV-infected individuals

Locher

Vanham

Kestens

et al. 1994

Clinical and Experimental Immunology

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SUMMARY The expression and co‐expression profiles of functionally important monocyte surface markers were compared between control and HIV+ individuals using combined physical gating and dim CD4 expression to delineate the monocytes. The FcγRII (CD32), the MHC class II antigen HLADR and the adhesion molecules CDIIa (LFA‐1α), CD18 and CD54 (ICAM‐1) showed an unimodal distribution. Of these markers, CDI Ia and HLA‐DR were up‐regulated in the HIV+ subjects compared with controls. The expression levels of the adhesion molecules correlated with each other in both patients and controls. The CD11b (CR3‐α), CD14, FcγRI, and FcγRIII markers were bimodally distributed. Compared with controls, monocytes from seropositives contained fewer CDbright+ cells, an equal proportion of FcγIbright+ cells, but twice as many FCγ RIII+ cells. The expression level of FcγRI and CD11b within their brightly positive subset increased as CD4T cells decreased. Both in patients and controls, co‐expression of bright CD11b, CD14 and FCγRI was shown, whereas the FcγRIII+ cells were negative or dim positive for the former triad. We conclude that the expression of two FcγR (I and III), of the adhesion molecules CD11a and CD11b and of HLA‐DR showed particular alterations on monocytes from HIV+ subjects. The relationship of these phenotypic observations with altered cytokine profiles and altered monocyte function is discussed.

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“…Studies of monocytes (37)(38)(39)(40) and alveolar M (39) from HIVϩ individuals have reported normal levels of CD11b, and CD11c has been found to be both decreased (40) and increased (37, 41) on monocytes from AIDS patients. Monocytes from asymptomatic HIVϩ individuals have been found to have increased levels of CD11a, CD11b, and CD11c (41,42).…”

Section: Discussionmentioning

confidence: 99%

Modulation of the effector function of human macrophages for Histoplasma capsulatum by HIV-1. Role of the envelope glycoprotein gp120.

Chaturvedi

Newman²

1997

J. Clin. Invest.

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We have demonstrated that monocyte-derived macrophages (M ) from HIV ϩ individuals are deficient in their capacity to phagocytose Histoplasma capsulatum (Hc) yeasts, and are more permissive for the intracellular growth of Hc. To determine whether these defects in M function were caused by HIV infection of the M and/or by pathological events associated with HIV infection, cultured normal human M were infected with the HIV-1 BaL strain. Virus production, quantified by reverse transcriptase activity and p24 antigen, was evident on day 8 after infection and peaked on day 16. On days 12, 16, and 20 after infection, HIV-1-infected M were deficient in their capacity to recognize and bind Hc yeasts compared with control M , and also were more permissive for the intracellular growth of Hc. Culture of normal M with the envelope glycoprotein gp120 inhibited phagocytosis of Hc yeasts by M in a concentration-dependent manner, but did not cause more rapid intracellular growth of Hc. Normal M cultured in the serum of HIV ϩ individuals with impaired M function subsequently were deficient in their capacity to phagocytose Hc yeasts, and were more permissive for the intracellular growth of yeasts compared with M cultured in normal serum. Conversely, culture of normal M in the serum of HIV ϩ patients with normal M function did not affect the interaction of Hc yeasts with M . Moreover, when M from HIV ϩ individuals that were initially defective in host defense against Hc were cultured in normal HIV Ϫ serum, normal M function was demonstrated. Adsorption of gp120 from the serum of two HIV ϩ patients removed the capacity of the serum to cause a M defect in phagocytosis of Hc, but had no effect on the capacity of the serum to cause accelerated intracellular growth. These data demonstrate that observed defects in M interaction with Hc yeasts may be caused by gp120 and other, as yet unknown serum component(s) probably released into serum by HIV-infected cells. (

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Monocyte Phenotype and Function in Patients with the Acquired Immunodeficiency Syndrome (AIDS) and AIDS‐Related Disorders

Cited by 42 publications

References 32 publications

Expression patterns of Fcγ receptors, HLA-DR and selected adhesion molecules on monocytes from normal and HIV-infected individuals

Modulation of the effector function of human macrophages for Histoplasma capsulatum by HIV-1. Role of the envelope glycoprotein gp120.

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